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F18
PASSIVE TRANSFER OF IgG FROM HORSES WITH ALOPECIA AREATA-LIKE
HAIR LOSS
1Gardner
SH, 2Olivry
T, 1Lindsey
NJ and 1Tobin
DJ. 1Dept.
of Biomedical Sciences, University of Bradford, West Yorkshire,
England. 2College
of Veterinary Medicine, North Carolina State University, Raleigh,
NC, USA.
Alopecia areata (AA) is a presumptive autoimmune hair loss
disorder affecting humans and several other mammalian species.
Recently we have demonstrated the presence of anti-hair follicle
(HF) auto-antibodies in humans, horses and dogs with AA as
well as in the C3H/HeJ AA mouse model. However, it is unclear
whether these antibodies are pathogenic; some suggest they
result secondary to follicular damage. Previously, we reported
limited telogen arrest and shedding in murine skin after passive
transfer of equine AA whole serum and now extend this investigation
by passively transferring purified equine AA IgG into murine
haired skin. Sera used for this study were selected on the
basis of high titer anti-HF antibodies by indirect immunofluorescence
and western blotting and were re-tested after IgG purification.
Anagen III/IV C57Bl/10 murine skin was injected intradermally
with 5mg
IgG twice weekly for 44 days. Thereafter, dorsum skin was
harvested at both 7 hours and 10 days post final injection
for H&E staining. Full hair regrowth was observed around
the injection site in all mice by 12 days post first injection.
However, the injection site itself remained hairless for a
further 14 days in mice treated with normal IgG but did not
regrow until 37 days later in mice treated with AA IgG. H&E
stained sections of AA IgG-treated peri-injection site skin
revealed a spatially-restricted loss of hair follicles associated
with the massive mixed-cell inflammatory infiltrate located
around the hair follicles and in the dermis. Other notable
findings included epidermal thickening and cyst formation.
None of these features was observed in normal IgG-treated
skin. While this study suggests that AA IgG injected into
murine haired-skin can have local negative effects on hair
growth consistent with an inflammatory response, a pathogenic
role for anti-hair follicle antibodies in AA awaits confirmation.
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